臭氧油通过抑制 FcεRI/Syk 信号通路缓解二硝基氯苯诱导的过敏性接触性皮炎。
Ozonated oil alleviates dinitrochlorobenzene-induced allergic contact dermatitis via inhibiting the FcεRI/Syk signaling pathway.
机构信息
Department of Dermatology, Third Xiangya Hospital, Central South University, Changsha 410013.
Medical Ozone Research Center of Central South University, Changsha 410013.
出版信息
Zhong Nan Da Xue Xue Bao Yi Xue Ban. 2023 Jan 28;48(1):1-14. doi: 10.11817/j.issn.1672-7347.2023.220082.
OBJECTIVES
Ozone is widely applied to treat allergic skin diseases such as eczema, atopic dermatitis, and contact dermatitis. However, the specific mechanism remains unclear. This study aims to investigate the effects of ozonated oil on treating 2,4-dinitrochlorobenzene (DNCB)-induced allergic contact dermatitis (ACD) and the underling mechanisms.
METHODS
Besides the blank control (Ctrl) group, all other mice were treated with DNCB to establish an ACD-like mouse model and were randomized into following groups: a model group, a basal oil group, an ozonated oil group, a FcεRI-overexpressed plasmid (FcεRI-OE) group, and a FcεRI empty plasmid (FcεRI-NC) group. The basal oil group and the ozonated oil group were treated with basal oil and ozonated oil, respectively. The FcεRI-OE group and the FcεRI-NC group were intradermally injected 25 µg FcεRI overexpression plasmid and 25 µg FcεRI empty plasmid when treating with ozonated oil, respectively. We recorded skin lesions daily and used reflectance confocal microscope (RCM) to evaluate thickness and inflammatory changes of skin lesions. Hematoxylin-eosin (HE) staining, real-time PCR, RNA-sequencing (RNA-seq), and immunohistochemistry were performed to detct and analyze the skin lesions.
RESULTS
Ozonated oil significantly alleviated DNCB-induced ACD-like dermatitis and reduced the expressions of IFN-γ, IL-17A, IL-1β, TNF-α, and other related inflammatory factors (all P<0.05). RNA-seq analysis revealed that ozonated oil significantly inhibited the activation of the DNCB-induced FcεRI/Syk signaling pathway, confirmed by real-time PCR and immunohistochemistry (all P<0.05). Compared with the ozonated oil group and the FcεRI-NC group, the mRNA expression levels of IFN-γ, IL-17A, IL-1β, IL-6, TNF-α, and other inflammatory genes in the FcεRI-OE group were significantly increased (all P<0.05), and the mRNA and protein expression levels of FcεRI and Syk were significantly elevated in the FcεRI-OE group as well (all P<0.05).
CONCLUSIONS
Ozonated oil significantly improves ACD-like dermatitis and alleviated DNCB-induced ACD-like dermatitis via inhibiting the FcεRI/Syk signaling pathway.
目的
臭氧被广泛应用于治疗湿疹、特应性皮炎和接触性皮炎等过敏性皮肤疾病。然而，其具体机制尚不清楚。本研究旨在探讨臭氧油治疗 2,4-二硝基氯苯（DNCB）诱导的过敏性接触性皮炎（ACD）的作用及其潜在机制。
方法
除空白对照组（Ctrl 组）外，其余所有小鼠均用 DNCB 处理以建立 ACD 样小鼠模型，并随机分为以下几组：模型组、基础油组、臭氧油组、FcεRI 过表达质粒（FcεRI-OE）组和 FcεRI 空质粒（FcεRI-NC）组。基础油组和臭氧油组分别给予基础油和臭氧油处理。FcεRI-OE 组和 FcεRI-NC 组在给予臭氧油处理时，分别皮内注射 25μg FcεRI 过表达质粒和 25μg FcεRI 空质粒。我们每天记录皮肤病变情况，并使用反射共聚焦显微镜（RCM）评估皮肤病变的厚度和炎症变化。进行苏木精-伊红（HE）染色、实时 PCR、RNA 测序（RNA-seq）和免疫组织化学染色，以检测和分析皮肤病变。
结果
臭氧油显著减轻 DNCB 诱导的 ACD 样皮炎，并降低 IFN-γ、IL-17A、IL-1β、TNF-α 等相关炎症因子的表达（均 P<0.05）。RNA-seq 分析显示，臭氧油显著抑制 DNCB 诱导的 FcεRI/Syk 信号通路的激活，实时 PCR 和免疫组织化学染色也证实了这一点（均 P<0.05）。与臭氧油组和 FcεRI-NC 组相比，FcεRI-OE 组 IFN-γ、IL-17A、IL-1β、IL-6、TNF-α 等炎症基因的 mRNA 表达水平显著升高（均 P<0.05），FcεRI-OE 组 FcεRI 和 Syk 的 mRNA 和蛋白表达水平也显著升高（均 P<0.05）。
结论
臭氧油通过抑制 FcεRI/Syk 信号通路，显著改善 ACD 样皮炎，减轻 DNCB 诱导的 ACD 样皮炎。
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